Guillain-Barre Syndrome: Causes, Symptoms, Treatment and Recovery

A number of diseases develop as a secondary reaction of human immunity to an infectious agent. They are accompanied by the destruction of neurons and the violation of nervous regulation. The most severe course is Guillain-Barre syndrome( GBS or autoimmune polyneuropathy).

Definition of the disease

It is characterized by inflammatory processes, destruction of the upper protective( myelin) layer of nerves of the peripheral system. It is considered as a result of the pathological immune reaction of the organism, provoked by the transferred disease of infectious etiology. Infection can be caused by a number of herpes viruses, mycoplasmas, a hemophilic rod.

GBS is the main cause( after poliomyelitis) of paresis of peripheral nerves( flaccid paralysis) in children. According to statistics, men are more likely to suffer from GBS than women.


The virus origin of the disease is discussed. The proof of this theory could be the isolation of the viral culture of an individual pathogen of GBS.

The allergic cause of the development of autoimmune polyneuropathy is more often considered. As evidence, the results of laboratory studies of the occurrence of SGB in animals are presented.

An experimental animal was given an emulsion obtained from diseased peripheral nerve trunks as an antigen. After the injection, all typical symptoms of autoimmune polyneuropathy were observed. In the acute period of the current in the blood fetuses of injected animals, the changes in the immunity parameters( humoral and cellular) were traced.

The theory of the autoimmune cause of the development of GBS is generally accepted. At the same time, the body's immunity reacts to cells of the own nervous system as to foreign bodies. Mistakenly recognizes the causative agent of infection in them, destroying the upper myelinated layer of neurons with the help of leukocytes and macrophages.

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Possible pathogenesis and causes of

development The etiology of the origin of GBS is not established. It is generally accepted to consider the autoimmune nature of the disease and the associated course of pathogenesis. Development of SGB is preceded by an infectious disease or vaccine( from poliomyelitis, diphtheria).

More often the pathogenesis of autoimmune polyneuropathy is observed after acute acute infectious inflammation in the small intestine. Or, as a consequence, the manifestation of HIV infection.

After 10-14 days after recovery, the pathogenesis of GBS begins. The transferred infection provokes the development of secondary immunity.

An autoimmune reaction occurs on the auxiliary cells of the nerves of the lemocytes. They are responsible for the construction of the myelin layer of the nerve, its nutrition, fix the position of the neuron axon.

The defeat of lemocytes is accompanied by the formation of edema, the saturation of the lymph of certain parts of the nerves. Segmental lesions are observed with pronounced destruction of the myelin layer.

The aggravation of the course of the pathogenesis of GBS is associated with a disruption in the metabolism( nutrition) of neurons. Lemmatocytes from above are covered with a membrane consisting of lipids.

An autoimmune reaction in the flow of GBS leads to the destruction of the cell membrane. In the blood, the concentration of decomposition products of the lipid shell and their constituents is observed.

The thinning of the cell membrane increases its penetrating ability. Affected areas of the nerve tissue are impregnated with lymph and blood.

Predisposing causes of development of SGB:

  • Surgical operations.
  • Viral or infectious diseases.
  • Inflammation of the parotid gland.
  • Lymphoma.
  • Vaccination.

Symptoms of

There are such forms of the course of GBS:

  • Acute - symptoms are manifested for several days.
  • Subacute current - 2-3 weeks.
  • Chronic - ten days - several months.

The primary manifestation of GBS is associated with the manifestation of symptoms of a viral respiratory infection:

  • Catarrh of the respiratory tract.
  • Feeling of total fatigue and malaise.
  • Ultimate increase in body temperature.
  • Disorders of the bowel and stomach.

An indication of the destruction of nerve cells at the onset of the disease is the growing weakening of the limb muscles. First, the lower parts of the lower leg are affected. Hands can remain unaffected throughout the entire course of the SGB.

Further manifestations associated with the destruction of the structure of neurons are accompanied by a decrease in the sensitivity of individual sections of the limbs. There are muscle pains in the shoulder region, pelvis, back. The weakening of innervation of muscles is symmetrical.

Abnormal protrusion of the abdomen is observed. The abdominal type of respiration prevails, in which the muscles of the chest are more involved. As a result, the weakening of the innervation of the diaphragm is a violation of inspiration-exhalation.

Violations in the activity of internal organs are pronounced in the acute course of GBS.They are manifested by increased pressure( arterial), a violation of the process of separation of sweat. Heart rhythm changed. Accompanied by increased or slowed heart rate, arrhythmia.

Forms of

SGB The main classification of Guillain-Barre syndrome:

  • Classical - characterized by inflammatory processes, destruction of the myelin layer of lemocytes.
  • Axonal form - not only lemocytes, but also the processes of nerve cells( axons) are affected. It manifests itself as symptoms of motor and motor function disorders.
  • Motor-sensory - reduction in tone and motor impairment, symmetrical muscle weakness, purulent inflammation of the conjunctiva of the eye.
  • Miller-Fisher Syndrome - manifested by impaired vision, paresis of the facial nerve. Diagnosed in 75% of children with GBS.

Treatment of

For the diagnosis of GBS, symptomatic treatment is primarily used. The manifestation of signs of violation of breathing, swallowing and cardiac activity requires urgent hospitalization.

Patients are connected to a respirator. Apply plasmapheresis. If swallowing is difficult, the respiratory tube is inserted into the trachea and the nasogastric tube. Constipation is treated with a laxative.

With stagnant processes for urinary outflow, bladder catheterization is performed. Antibiotics are injected with infections of the trachea or bronchus, bladder and urogenital canals.

To prevent thrombosis of the veins of the lower leg, heparin is used. When the facial nerve is damaged and the motor function of facial muscles is weakened - eye drops( from the drying of the cornea).

In the treatment of pediatric GBS, human immunoglobulin or plasmapheresis is injected intravenously. Assign medicines to reduce the level of immunity( immunosuppressants).

Traditional medicine in the treatment of SPB is rarely used.

Her recipes are based on the methods of physiotherapy and apitherapy:

  • Medicinal baths based on herbal decoctions( sage, motherwort).
  • Barefoot bare stems of stinging nettle.
  • Ointments and creams based on bee venom.

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Rehabilitation and rehabilitation of

Almost 60% of patients experience atony( lethargy) of skeletal muscles.

Therefore, rehabilitation activities are applicable even in the early stages of the SGB.

  • Massage.
  • Therapeutic gymnastics.
  • Application paraffin.
  • Electrophoresis.
  • Radon baths.

With timely treatment, 70% of patients with GBS completely recover. Only in 5% of patients the disease passes into the chronic form and its repeated manifestation( relapses) is observed. In our time, mortality from the SGB has been reduced to 5%.

The course of the disease is dangerous by breaking the innervation of many systems. Later, diagnosis and untimely hospitalization can lead to the death of the patient. Treatment should be started when the first symptoms occur.

The photo shows what happens to the nerves in the Gineina-Barre syndrome:

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